The goal of this proposal is to improve the vestibular implant?s ability to reduce the vestibular-dependent perceptual, postural, and visual symptoms that affect patients with severe peripheral vestibular damage. We will achieve this goal by investigating how the brain processes acute vestibular signals provided by the vestibular implant (VI) and by determining how central processing changes after sub-acute (8 hours) exposure to motion-modulated VI stimulation. Aim 1 focuses on the brain?s ability to extract and process spatial information provided by the VI within an inherently noisy neural environment and to synthesize it with other motion cues such as those derived from visual flow. We will take advantage of the VI?s unique ability to titrate noise levels on vestibular afferents to determine how information transfer from the VI to the brain can be maximized and to investigate how vestibular reliability affects the integration of vestibular and visual spatial information. We also will utilize the VI?s unique ability to provide vestibular motion cues to patients who chronically lack these inputs to determine how the brain re-weighs visual spatial information when vestibular signals are absent, how this leads to visually-mediated imbalance and dizziness, and how re-introducing vestibular information with the VI can alleviate this problem by reducing the brain?s dependence on visual information. Aim 2 focuses on the brain?s ability to re-calibrate its internal model of the labyrinth when the vestibular periphery is suddenly changed by activating the VI, as reflected in the assessment of behaviors that require resolution of sensory ambiguities (active vs. passive motion, tilt vs. translation discrimination). We propose that when the VI is activated the internal model of the labyrinth will be inaccurate, resulting in mis- estimates of external perturbation during voluntary head rotation evidenced by slowing of head rotations and aberrant activation of antagonist muscles, and that the brain will adapt during chronic stimulation to incorporate the VI into its internal model, which will normalize head motion dynamics and the pattern of neck muscle activation. Furthermore, we propose that off-vertical head rotations will lead to aberrant estimates of linear acceleration because the gravito-inertial force (GIF) sensed by the otoliths/graviceptors will not accurately reflect the estimate of head tilt generated by integration of the VI rotational signal, but that this will normalize over time as the brain re-calibrates the relationship between GIF and estimates of gravity mediated by VI inputs. Aim 3 focuses on perception and oculomotor and postural reflexes, the acute changes after the VI is activated, adaptation during VI stimulation, and the relationship between reflex adaptation and changes in neural processing. We propose that perception, eye movements and posture will improve substantially when the VI is activated, and that adaptation will improve these responses during sub-acute stimulation. In sum, we aim to improve the efficacy of the VI in human subjects by developing new knowledge about how the brain processes motion cues provided by the VI and correlating this information with behavioral outcomes.